Sun Ru Bao, Xi Zhu Ge, Zhang Hua Shan, Zhang Wei
Beijing Institute of Disease Control and Prevention, Beijing 100071, China; Tianjin Institute of Health and Environmental Medicine, Tianjin 300050, China; Tianjin Key Laboratory of Risk Assessment and Control for Environmental and Food Safety, Tianjin 300050, China.
Tianjin Institute of Health and Environmental Medicine, Tianjin 300050, China; Tianjin Key Laboratory of Risk Assessment and Control for Environmental and Food Safety, Tianjin 300050, China.
Biomed Environ Sci. 2014 Feb;27(2):122-5. doi: 10.3967/bes2014.026.
Information regarding decabromodiphenyl ethane (DBDPE) effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.
关于十溴二苯醚（DBDPE）对肝毒性和代谢影响的信息有限。在本研究中，给Wistar大鼠口服不同剂量的DBDPE。DBDPE诱导氧化应激，升高血糖水平，增加CYP2B2 mRNA、CYP2B1/2蛋白、7-戊氧基试卤灵O-脱戊基酶（PROD）活性，并诱导CYP3A2 mRNA、CYP3A2蛋白和荧光素苄基醚脱苄基酶（LBD）活性。UDPGT活性随其暴露水平的增加而增加，表明口服DBDPE暴露通过CAR/PXR信号通路诱导大鼠体内的药物代谢酶。细胞色素P450酶（CYPs）和II相生物转化的共同调节酶的诱导可能会影响内源性底物的稳态，包括甲状腺激素，这反过来可能会改变葡萄糖代谢。
